Bouras Georgios, Giannopoulos Georgios, Hatzis George, Alexopoulos Dimitrios, Leventopoulos George, Deftereos Spyridon
Cardiology Department and Cardiac Catheterization Laboratory, Athens General Hospital "G. Gennimatas", Mesogeion 154, 11527, Athens, Greece.
Med Chem. 2014;10(7):682-99. doi: 10.2174/1573406410666140318113325.
Heart failure (HF) is a complex heterogeneous syndrome with immune, metabolic and neurohumoral mechanisms interacting and leading to gradual heart contractility impairment. From the first study-to correlate inflammation with HF, inflammation biomarkers have been the subject of intense inquiry in patients with various forms of HF. Chronic HF (CHF) is strongly associated with inflammation in terms of pathogenesis, progression, severity and prognosis. Inflammatory mediators participate in CHF pathophysiology in various ways like exerting direct impact on cardiac myocytes, fibroblasts and β-adrenergic receptors leading to hypertrophy, fibrosis and impaired cardiac contractility, respectively, or inducing apoptosis by stimulation of the proper genes. The anti-inflammatory effects of classical heart failure therapeutic strategies such as ACEI and b-blockers are rather conflicting. Whether novel immunomodulating and anti-inflammatory therapeutic approaches should be added to existing therapies in order to ensure additional benefit to HF patients is under investigation. In this review, we summarize the pathophysiological link between inflammatory processes and CHF, focusing on the role of novel and traditional inflammatory biomarkers and highlighting novel anti-inflammatory therapeutic strategies.
心力衰竭（HF）是一种复杂的异质性综合征，免疫、代谢和神经体液机制相互作用，导致心脏收缩力逐渐受损。从第一项将炎症与HF相关联的研究开始，炎症生物标志物就一直是各种形式HF患者深入研究的主题。慢性HF（CHF）在发病机制、进展、严重程度和预后方面与炎症密切相关。炎症介质以多种方式参与CHF的病理生理学，例如对心肌细胞、成纤维细胞和β-肾上腺素能受体产生直接影响，分别导致肥大、纤维化和心脏收缩力受损，或通过刺激相关基因诱导细胞凋亡。经典心力衰竭治疗策略如ACEI和β受体阻滞剂的抗炎作用相当矛盾。是否应将新型免疫调节和抗炎治疗方法添加到现有治疗中以确保给HF患者带来额外益处仍在研究中。在本综述中，我们总结了炎症过程与CHF之间的病理生理联系，重点关注新型和传统炎症生物标志物的作用，并强调新型抗炎治疗策略。
